Does transcription factor, induced by daptomycin and vancomycin, affect HIF-1α, Chondroadherin, and COL2A1?
Yaşar Şirin, Duygu
Kaya, Yasin Emre
Gümüştaş, Seyit Ali
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CitationKaraarslan, N., Yılmaz, İ., Yaşar Şirin, D., Özbek, H., Kaya, Y. E., Akyuva, Y. ... Erdem, İ. (2018). Does transcription factor, induced by daptomycin and vancomycin, affect HIF-1α, Chondroadherin, and COL2A1? Annals of Medical Research, 25(4), 756-762. https://doi.org/10.5455/annalsmedres.2018.06.110
Aim: In this study, it was firstly aimed to investigate the effect of Daptomycin (DAP) on the proliferation in Vancomycin (VCM)-administered primary chondrocyte cultures and non-drug-administered primary chondrocyte cultures. Our second objective was to investigate the effects of DAP and VCM on the NP-specific marker protein chondroadherin (CHAD), which is associated with spinal cord and dorsal column growth, on the transcription factor-1 alpha (HIF-1α), which is induced by hypoxia, and on a type II collagen (COL2A1), which is also known to play a significant role in the development of extracellular matrix, at the pharmaco-molecular level. Material and Methods: Standard human primary chondrocyte cultures were established. DAP and VCM were added to the samples. In all groups, molecular analysis was performed at 0th, 24th and 48th hours. In addition, the surface morphology of the cells was evaluated. Results: Changes in cell morphology and cell death in cultures were observed 24 hours after administration of antibiotics to cell cultures. It was observed that drug administration was associated with the cell viability and that cell viability rate for two antibiotics was similar at the 0th and 48th hours. The expression of three genes decreased at the 24th hour in the experimental group where DAP was administered. Conclusion: Thanks to this molecular-based research, it should not be forgotten that DAP and VCM active pharmacological agents, especially used in the treatment of Methicillin-resistant Staphylococcus aureus induced surgical infections, have a negative effect on human chondrocyte and ECM components.